摘要
The diabetic foot is characterised by painless foot ulceration and/or arthropathy;it is a typical complication of painless diabetic neuropathy.Neuropathy depletes the foot skin of intraepidermal nerve fibre endings of the afferent A-delta and C-fibres,which are mostly nociceptors and excitable by noxious stimuli only.However,some of them are cold or warm receptors whose functions in diabetic neuropathy have frequently been reported.Hence,it is well established by quantitative sensory testing that thermal detection thresholds at the foot skin increase during the course of painless diabetic neuropathy.Pain perception(nociception),by contrast,has rarely been studied.Recent pilot studies of pinprick pain at plantar digital skinfolds showed that the perception threshold was always above the upper limit of measurement of 512 m N(equivalent to 51.2 g) at the diabetic foot.However,deep pressure pain perception threshold at musculus abductor hallucis was beyond 1400 k Pa(equivalent to 14 kg;limit of measurement) only in every fifth case.These discrepancies of pain perception between forefoot and hindfoot,and between skin and muscle,demand further study.Measuring nociception at the feet in diabetes opens promising clinical perspectives.A critical nociception threshold may be quantified(probably corresponding to a critical number of intraepidermal nerve fibre endings),beyond which the individual risk of a diabetic foot rises appreciably.Staging of diabetic neuropathy according to nociception thresholds at the feet is highly desirable as guidance to an individualised injury prevention strategy.
The diabetic foot is characterised by painless footulceration and/or arthropathy; it is a typical complicationof painless diabetic neuropathy. Neuropathy depletesthe foot skin of intraepidermal nerve fibre endings of theafferent A-delta and C-fibres, which are mostly nociceptorsand excitable by noxious stimuli only. However, someof them are cold or warm receptors whose functionsin diabetic neuropathy have frequently been reported.Hence, it is well established by quantitative sensory testingthat thermal detection thresholds at the foot skin increaseduring the course of painless diabetic neuropathy. Painperception （nociception）, by contrast, has rarely beenstudied. Recent pilot studies of pinprick pain at plantardigital skinfolds showed that the perception thresholdwas always above the upper limit of measurement of 512mN （equivalent to 51.2 g） at the diabetic foot. However,deep pressure pain perception threshold at musculus abductor hallucis was beyond 1400 kPa （equivalent to 14 kg; limit of measurement） only in every fifth case. These discrepancies of pain perception between forefoot and hindfoot, and between skin and muscle, demand further study. Measuring nociception at the feet in diabetes opens promising clinical perspectives. A critical nociception threshold may be quantified （probably corresponding to a critical number of intraepidermal nerve fibre endings）, beyond which the individual risk of a diabetic foot rises appreciably. Staging of diabetic neuropathy according to nociception thresholds at the feet is highly desirable as guidance to an individualised injury prevention strategy.
